Acute respiratory failure (ARF) exists when
the patient's breathing apparatus fails in its ability to maintain arterial
blood gases within the normal range. By definition, ARF is present when
the blood gases demonstrate:

Hypoxaemia on its own does not always mean
respiratory failure, for example, if the subject is at altitude or has
a right to left shunt due to congenital heart disease.

We are concerned only with ARF, one of the
most dramatic and life threatening emergencies that the casualty officer
and the house office may have to deal with in the hospital setting.

Pathophysiology

Any part of the respiratory system may be
involved in the causation of a respiratory emergency, i.e.

The respiratory centre in the CNS

The respiratory apparatus (e.g. chest wall and lungs)

The respiratory muscles including the diaphragm, the main respiratory
pump

The gas exchanging units in the lung i.e. the respiratory bronchioles
and the alveoli

It is pertinent to remember that in assessing
patientís with ARF, most attention is paid to what is happening at the
alveolar level i.e. the blood gases

Examples of conditions
causing ARF are shown in Table 1

Clinical
Picture

The clinical picture
varies with the cause but any of those mentioned in Table 1 leads to a
deterioration in the patient's respiratory gas exchange. The subsequent
changes which occur in blood gases, particularly carbon dioxide, cause
stimulation of the medullary chemo-receptor and compensatory mechanisms
to be activated. The patient becomes aware of the necessity to breathe,
and as the precipitating cause progresses, exhibits overt signs of distress,
i.e. dyspnoea. Eventually blood gases can no longer be kept in the normal
range and ARF supervenes.

ARF resulting
from CNS depression as a result of drugs or injury does not produce overt
signs of respiratory distress. Accurate diagnosis is dependent on a high
index of suspicion and is confirmed by arterial blood gas analysis.

Generally, the
patient becoming anxious and completely preoccupied with the necessity
to concentrate every effort on ventilation heralds the onset of ARF. The
eyes are closed, the accessory muscles of ventilation are fully used;
often a characteristic position is adopted, such as sitting forward with
drooling secretions, as in the child with acute epiglottitis. Hypoxia
and hypercarbia produce characteristic effects on the CNS and cardiovascular
system (CVS), for example:

Diagnosis depends
on history, clinical examination and special investigations such as chest
X-ray, peak expiratory flow rate and arterial blood gas analysis. It is
important to establish the causative site (Table 1).

For example, the
history gives a clue to pre-existing disease such as chronic bronchitis
and asthma, or may distinguish between acute epiglottitis (sudden onset)
and laryngo-tracheobronchitis (slower onset over 24 hours), when the clinical
signs are equivocal. On clinical examination, expiratory wheeze suggests
intrathoracic airway obstruction whilst inspiratory wheeze suggests that
it is extrathoracic. Chest X-ray will reveal parenchymal causes such as
pneumonia, airway obstruction due to foreign bodies (ipsilateral hyperinflation
of lung), pleural and thoracic cage causes, such as effusion, pneumothorax
and fractured ribs. Raised bicarbonate levels in the blood gases suggest
chronic pre-existing disease, and a combination of hypoxia, hypocarbia
and an initial metabolic alkalosis followed by acidosis is a common accompaniment
of ARDS.

This applies particularly
to the unconscious patient, e.g. due to overdose, general anaesthesia,
CNS trauma and so on. The patient is placed on the side with the head
down, and lower jaw pulled forward to prevent the tongue falling back
and obstructing the upper airway. At this stage it may become obvious
that the obstruction is due primarily to foreign bodies or vomit, so this
must be cleared, if possible.

Indications
for artificial airways

(1)Oropharyngeal:
this is useful where it is expected that the patient will soon recover
consciousness, e.g. post-operatively, or where there is lack of expertise
in endotracheal intubation. A laryngeal mask may be used as an alternative
in this situation

(2)Endotracheal
tube (ETt): If unconsciousness
is expected to last for more than a matter of minutes, as in drug overdose,
then an ETT must be used both to ensure and to protect the airway (e.g.
from aspiration of gastric contents). If ventilation is depressed or inadequate
due to trauma or disease, than mechanical ventilation will be required.

(3)Cricothyrotomy
and tracheostomyobstruction above the
cords due to disease or infection may make intubation impossible. Cricothyrotomy
or tracheostomy is then necessary to restore the airway.

(4)Bronchoscopymay also be required for bronchial toilet, removing
viscid mucous and obtaining specimens for microscopy and culture

It is of paramount
importance to maintain a PaO2 sufficient to give an arterial Hb saturation
of at least 85% (i.e. 8-9 kPa or 60-70 mmHg). Hyperoxia should be avoided,
particularly in the bronchitic who is a CO2 retainer and dependent on
hypoxic ventilatory drive.

(c)
Maintain alveolar ventilation and treat underlying cause

These two are inextricably
linked. The causes of ARF are many and varied as are the requisite therapies.
If treatment of the underlying cause is not successful (i.e. steroids,
bronchodilators in asthma; physiotherapy, antibiotics, mucolytics, bronchodilators
in acute or chronic bronchitis), then the carbon dioxide tension will
begin to rise, necessitating intermittent positive pressure ventilation
(IPPV). There is little place for respiratory stimulants, except perhaps
narcotic antagonists in opiate overdose. NB Infection is a cause of exacerbation
of ARF in bronchitics in less than 50% of cases. Other causes such as
heart failure, dysrthymias and pneumothorax must be excluded and treated
where necessary.

In ARF due to chronic
obstructive pulmonary disease (COPD), muscle fatigue is a major contributory
factor to continuing hypoxia and hypercarbia. Non-invasive methods of
ventilation (e.g. nasal mask) as well as endotracheal intubation and IPPV
may be needed.

SPECIAL PROBLEMS ENCOUNTERED IN THE INTENSIVE
CARE UNIT (ICU)

Despite the fact
that there are many causes of ARF, anaesthetists in ICU are faced with
a relatively small number of problems, which occur frequently.

(a)
The croup syndrome

Upper airway obstruction
in the small child represents one of the most life-threatening situations
in clinical medicine. Croup means literally 'noisy breathing' and is due
to upper airway obstruction, conventionally delineated into supra-and
subglottic. The most common causes are infectious and traumatic.

(1)
Infectious

Supraglottic obstruction
is usually due to epiglottitis. The main features of the disease are rapid
onset of severe respiratory obstruction and a high temperature with the
patient adopting the classical sitting position with drooling secretions.

The diagnosis
is made on the history and clinical findings, and as the child (usually
3 to 7 years old) may completely obstruct at any time, he or she must
be taken immediately to the operating theatre with an experienced anaesthetist
and surgeon prepared for endotracheal intubation (ETI) or tracheotomy.
This is usually performed under general anaesthesia as attempted manipulations
to visualise the epiglottis in the awake patient often results in total
obstruction and death. Following preferably nasotracheal intubation, the
child is sedated and treated for Haemophilus influenzae infection with
ampicillin and other appropriate antibiotics together with humidification
of inspired gases.

Subglottic
obstruction is usually due to laryngotracheobronchitis, with a much more
slowly progressive course, lower temperature and fewer signs of respiratory
obstruction. Intubation is required more rarely, and less often in a hurry.
However, the clinical course is often more protracted and, once instituted,
ETI is needed for longer periods than with epiglottitis.

The incidence of
both has decreased markedly in the last decade.

(2)
Trauma

This may be due
to instrumentation (eg post-extubation), inhalation of a foreign body,
external trauma or aspiration of noxious substances such as acid or alkali.
The history will usually confirm the diagnosis. Treatment will depend
on the cause, but usually requires intubation and steroid administration,
and in the case of foreign body, operative removal with bronchoscopy.

(b)
Acute (status) asthma

By the time the
patient with an acute asthmatic attack reaches the ICU, the anaesthetist
is faced with one of the most difficult management problems. The patient
is often exhausted, tachycardic, hypoxic, hypercarbic, acidotic and dehydrated,
yet needs intubation and ventilation to restore reasonable blood gases.
Attempting to intubate the patient 'awake' may precipitate cardiovascular
collapse. Following intubation, ventilation is usually extremely difficult
necessitating high inflation pressures which can only be lowered by prolonging
inspiration, and yet air trapping requires that expiration is also prolonged.
This conundrum requires considerable compromise with ventilator settings
and can often only be accommodated by accepting relatively high PaCO2
levels.

(c)
The chronic bronchitic patient requiring ventilation

In a previous section
it was mentioned that the chronic bronchitic who presents in ARF may proceed,
despite optimal therapy, to the point where nasal mask and non invasive
ventilation or endotracheal intubation and mechanical ventilation (IPPV)
is required. In such cases it is paramount that the patient is assessed
as to the suitability of this form of treatment. This involves a thorough
history from the patient (or relatives) with particular regard to:

Only guidelines
can be given, but in cases where the patient has had frequent previous
admissions with IPPV treatment, progressive lung damage can be anticipated
so that further periods of IPPV may be unwarranted. This is also applicable
to cases where the patient is housebound and/or breathless at rest. However,
recent studies suggest that the patient with ARF due to COPD has as good
a chance of weaning from mechanical ventilation s a patient who needs
IPPV from an acute attack of asthma.

(d)
Adult Respiratory Distress Syndrome (ARDS)

In recent years,
it has become evident that the lung can be injured primarily (as in aspiration
pneumonitis) as well as by a secondary process in severe illness or trauma.
Generally speaking it is the vascular endothelium (either bronchial venular
or capillary) which is affected. Damage from any of the causes below results
in loss of membrane integrity and thus increased permeability to fluid
and protein. This leaks into the interstitial space and lymphatics, producing
an exudative 'non' cardiogenic pulmonary oedema', with a characteristic
'fluffy' appearance on chest X-ray. It is distinguished from 'cardiogenic
pulmonary oedema', by demonstration of a normal or low pulmonary capillary
wedge pressure, and from oedema due to a low colloid oncotic pressure
by demonstration of a serum albumin of >30 g l-1. A pronounced decrease
in functional residual capacity (FRC) and compliance occurs, with a resulting
increased work of breathing and dyspnoea. This together with the associated
vascular damage results in an imbalance of ventilation and perfusion,
with hypoxia and increase in dead space. A pronounced inflammatory and
fibrotic stage may supervene and lead to permanent lung damage.

The symptoms are
those of severe ARF with dyspnoea being prominent. The 'clinical' condition
of the patient may not immediately give cause for concern, e.g. in early
'fat embolism'. However, sampling of the arterial blood gases reveals
profound hypoxaemia (PaO2 < 5 kPa or 35 mmHg) and secondary hyperventilation
with a low PaCO2 (< 4 kPa or 30 mmHg). If left untreated, CO2 retention
and metabolic acidosis develop. The profound hypoxia is often unresponsive
to additional oxygen by mask, in which case ETI with IPPV and positive
end expiratory pressure (PEEP) is required. The latter works by increasing
FRC by backward distending pressure thus reducing V/Q mis-match and improving
compliance at the same time.